Chapter 13. Memory and Learning

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Diana Kwon Santiago Ramón y Cajal revolutionized neurobiology in the late nineteenth century with his exquisitely detailed illustrations of neural tissues. Created through years of meticulous microscopy work, the Spanish physician-scientist’s drawings revealed the unique cellular morphology of the brain. “With Cajal’s work, we saw that the cells of the brain don’t look like the cells of every other part of the body — they have incredible morphologies that you just don’t see elsewhere,” says Evan Macosko, a neuroscientist at the Broad Institute of MIT and Harvard in Cambridge, Massachusetts. Ramón y Cajal’s drawings provided one of the first clues that the keys to understanding how the brain governs its many functions, from regulating blood pressure and sleep to controlling cognition and mood, might lie at the cellular level. Still, when it comes it comes to the brain, crucial information remained — and indeed, remains — missing. “In order to have a fundamental understanding of the brain, we really need to know how many different types of cells there are, how are they organized, and how they interact with each other,” says Xiaowei Zhuang, a biophysicist at Harvard University in Cambridge. What neuroscientists require, Zhuang explains, is a way to systematically identify and map the many categories of brain cells. Now researchers are closing in on such a resource, at least in mice. By combining high-throughput single-cell RNA sequencing with spatial transcriptomics — methods for determining which genes are expressed in individual cells, and where those cells are located — they are creating some of the most comprehensive atlases of the mouse brain so far. The crucial next steps will be working out what these molecularly defined cell types do, and bringing the various brain maps together to create a unified resource that the broader neuroscience community can use. © 2023 Springer Nature Limited

Keyword: Brain imaging; Development of the Brain
Link ID: 28880 - Posted: 08.24.2023

By Lauren Leffer When a nematode wriggles around a petri dish, what’s going on inside a tiny roundworm’s even tinier brain? Neuroscientists now have a more detailed answer to that question than ever before. As with any experimental animal, from a mouse to a monkey, the answers may hold clues about the contents of more complex creatures’ noggin, including what resides in the neural circuitry of our own head. A new brain “atlas” and computer model, published in Cell on Monday, lays out the connections between the actions of the nematode species Caenorhabditis elegans and this model organism’s individual brain cells. With the findings, researchers can now observe a C. elegans worm feeding or moving in a particular way and infer activity patterns for many of the animal’s behaviors in its specific neurons. Through establishing those brain-behavior links in a humble roundworm, neuroscientists are one step closer to understanding how all sorts of animal brains, even potentially human ones, encode action. “I think this is really nice work,” says Andrew Leifer, a neuroscientist and physicist who studies nematode brains at Princeton University and was not involved in the new research. “One of the most exciting reasons to study how a worm brain works is because it holds the promise of being able to understand how any brain generates behavior,” he says. “What we find in the worm forms hypotheses to look for in other organisms.” Biologists have been drawn to the elegant simplicity of nematode biology for many decades. South African biologist Sydney Brenner received a Nobel Prize in Physiology or Medicine in 2002 for pioneering work that enabled C. elegans to become an experimental animal for the study of cell maturation and organ development. C. elegans was the first multicellular organism to have its entire genome and nervous system mapped. The first neural map, or “connectome,” of a C. elegans brain was published in 1986. In that research, scientists hand drew connections using colored pencils and charted each of the 302 neurons and approximately 5,000 synapses inside the one-millimeter-long animal’s transparent body. Since then a subdiscipline of neuroscience has emerged—one dedicated to plotting out the brains of increasingly complex organisms. Scientists have compiled many more nematode connectomes, as well as brain maps of a marine annelid worm, a tadpole, a maggot and an adult fruit fly. Yet these maps simply serve as a snapshot in time of a single animal. They can tell us a lot about brain structure but little about how behaviors relate to that structure. © 2023 Scientific American

Keyword: Brain imaging; Development of the Brain
Link ID: 28879 - Posted: 08.24.2023

by Calli McMurray One of the co-directors of a now-shuttered Maryland psychology clinic implicated in 18 paper retractions has retired, Spectrum has learned. Prior to her retirement, Clara Hill was professor of psychology at the University of Maryland in College Park. Headshot of Clara Hill. Recent retirement: Clara Hill retired from the University of Maryland in the midst of 18 paper retractions after a 49-year career. Starting on 1 June, the American Psychological Association (APA) retracted 11 papers by Hill and her university colleagues Dennis Kivlighan, Jr. and Charles Gelso over issues with obtaining participant consent. The publisher plans to retract six more papers by the end of the year, according to an APA representative. On 13 August, Taylor & Francis retracted an additional paper led solely by Hill. The research was conducted at the Maryland Psychotherapy Clinic and Research Lab, where Hill, Kivlighan and Gelso were co-directors. The clinic had shut down as of 1 June. When asked about the circumstances surrounding Hill’s retirement, a university spokesperson told Spectrum in an email, “Dr. Clara Hill retired from UMD effective July 1, 2023.” After Spectrum asked again about the circumstances, a spokesperson replied, “This is all we’ll have for you on the faculty member’s retirement — thanks!” Hill worked at the university for 49 years. As of 1 August, Hill’s faculty page did not mention her retirement. By 14 August, her position had been amended to “Professor (Retired),” and a notice of her retirement had been added to the beginning of her biography. Spectrum left two voicemails on Hill’s university office phone and emailed her university address with requests for comment but did not hear back. The 11 papers retracted by the APA appeared in the Journal of Counseling Psychology, Dreaming and Psychotherapy. The additional retractions will come from the same titles, according to an APA representative. Hill conducted all 11 studies, whereas Kivlighan and Gelso conducted 10 and 6, respectively. © 2023 Simons Foundation

Keyword: Autism
Link ID: 28877 - Posted: 08.24.2023

Saima May Sidik A protein involved in wound healing can improve learning and memory in ageing mice1. Platelet factor 4 (PF4) has long been known for its role in promoting blood clotting and sealing broken blood vessels. Now, researchers are wondering whether this signalling molecule could be used to treat age-related cognitive disorders such as Alzheimer’s disease. “The therapeutic possibilities are very exciting,” says geneticist and anti-ageing scientist David Sinclair at Harvard University in Boston, Massachusetts, who was not involved in the research. The study was published on 16 August in Nature. Young blood, old brains About a decade ago, scientists discovered that blood from young mice could restore youthful properties, including learning abilities, in older mice2,3. The idea captivated Saul Villeda, a neuroscientist at the University of California, San Francisco, and a co-author of the new study. He and his colleagues have since been trying to identify the components of blood that cause this rejuvenation. Several lines of evidence suggested that PF4 might be one of these components, including the fact that young mice have higher levels of this molecule in their blood than do older mice. Villeda and his colleagues tried injecting PF4 into aged mice without including other blood components. The researchers found that the ratios of various types of immune cell shifted to become more similar to what is typically seen in younger mice. Some immune cells also reverted to a more youthful pattern of gene expression. Although PF4 was not able to cross the blood–brain barrier, its effects on the immune system also led to changes in the brain, probably through indirect mechanisms. Old mice that received doses of PF4 showed decreases in damaging inflammation in the hippocampus — a part of the brain that’s particularly vulnerable to the effects of ageing. They also showed increases in the levels of molecules that promote synaptic plasticity (the capacity to alter the strength of connections between nerve cells). © 2023 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 28874 - Posted: 08.19.2023

By Alla Katsnelson Our understanding of animal minds is undergoing a remarkable transformation. Just three decades ago, the idea that a broad array of creatures have individual personalities was highly suspect in the eyes of serious animal scientists — as were such seemingly fanciful notions as fish feeling pain, bees appreciating playtime and cockatoos having culture. Today, though, scientists are rethinking the very definition of what it means to be sentient and seeing capacity for complex cognition and subjective experience in a great variety of creatures — even if their inner worlds differ greatly from our own. Such discoveries are thrilling, but they probably wouldn’t have surprised Charles Henry Turner, who died a century ago, in 1923. An American zoologist and comparative psychologist, he was one of the first scientists to systematically probe complex cognition in animals considered least likely to possess it. Turner primarily studied arthropods such as spiders and bees, closely observing them and setting up trailblazing experiments that hinted at cognitive abilities more complex than most scientists at the time suspected. Turner also explored differences in how individuals within a species behaved — a precursor of research today on what some scientists refer to as personality. Most of Turner’s contemporaries believed that “lowly” critters such as insects and spiders were tiny automatons, preprogrammed to perform well-defined functions. “Turner was one of the first, and you might say should be given the lion’s share of credit, for changing that perception,” says Charles Abramson, a comparative psychologist at Oklahoma State University in Stillwater who has done extensive biographical research on Turner and has been petitioning the US Postal Service for years to issue a stamp commemorating him. Turner also challenged the views that animals lacked the capacity for intelligent problem-solving and that they behaved based on instinct or, at best, learned associations, and that individual differences were just noisy data. But just as the scientific establishment of the time lacked the imagination to believe that animals other than human beings can have complex intelligence and subjectivity of experience, it also lacked the collective imagination to envision Turner, a Black scientist, as an equal among them. The hundredth anniversary of Turner’s death offers an opportunity to consider what we may have missed out on by their oversight. © 2023 Annual Reviews

Keyword: Learning & Memory; Evolution
Link ID: 28869 - Posted: 08.09.2023

By Yasemin Saplakoglu On warm summer nights, green lacewings flutter around bright lanterns in backyards and at campsites. The insects, with their veil-like wings, are easily distracted from their natural preoccupation with sipping on flower nectar, avoiding predatory bats and reproducing. Small clutches of the eggs they lay hang from long stalks on the underside of leaves and sway like fairy lights in the wind. The dangling ensembles of eggs are beautiful but also practical: They keep the hatching larvae from immediately eating their unhatched siblings. With sickle-like jaws that pierce their prey and suck them dry, lacewing larvae are “vicious,” said James Truman, a professor emeritus of development, cell and molecular biology at the University of Washington. “It’s like ‘Beauty and the Beast’ in one animal.” This Jekyll-and-Hyde dichotomy is made possible by metamorphosis, the phenomenon best known for transforming caterpillars into butterflies. In its most extreme version, complete metamorphosis, the juvenile and adult forms look and act like totally different species. Metamorphosis is not an exception in the animal kingdom; it’s almost a rule. More than 80% of the known animal species today, mainly insects, amphibians and marine invertebrates, undergo some form of metamorphosis or have complex, multistage life cycles. The process of metamorphosis presents many mysteries, but some of the most deeply puzzling ones center on the nervous system. At the center of this phenomenon is the brain, which must code for not one but multiple different identities. After all, the life of a flying, mate-seeking insect is very different from the life of a hungry caterpillar. For the past half-century, researchers have probed the question of how a network of neurons that encodes one identity — that of a hungry caterpillar or a murderous lacewing larva — shifts to encode an adult identity that encompasses a completely different set of behaviors and needs. Truman and his team have now learned how much metamorphosis reshuffles parts of the brain. In a recent study published in the journal eLife, they traced dozens of neurons in the brains of fruit flies going through metamorphosis. They found that, unlike the tormented protagonist of Franz Kafka’s short story “The Metamorphosis,” who awakes one day as a monstrous insect, adult insects likely can’t remember much of their larval life. Although many of the larval neurons in the study endured, the part of the insect brain that Truman’s group examined was dramatically rewired. That overhaul of neural connections mirrored a similarly dramatic shift in the behavior of the insects as they changed from crawling, hungry larvae to flying, mate-seeking adults. All Rights Reserved © 2023

Keyword: Learning & Memory
Link ID: 28860 - Posted: 07.27.2023

by Giorgia Guglielmi Mice with a mutation that boosts the activity of the autism-linked protein UBE3A show an array of behaviors reminiscent of the condition, a new study finds. The behaviors differ depending on whether the animals inherit the mutation from their mother or their father, the work also reveals. The results add to mounting evidence that hyperactive UBE3A leads to autism. Duplications of the chromosomal region that includes UBE3A have been associated with autism, whereas deletions and mutations that destroy the gene’s function are known to cause Angelman syndrome, which is characterized by developmental delay, seizures, lack of speech, a cheerful demeanor and, often, autism. “UBE3A is on a lot of clinicians’ radar because it is well known to be causative for Angelman syndrome when mutated or deleted,” says lead investigator Mark Zylka, professor of cell biology and physiology at the University of North Carolina at Chapel Hill. “What our study shows is that just because you have a mutation in UBE3A, it doesn’t mean that it’s going to be Angelman syndrome.” In the cell, UBE3A is involved in the degradation of proteins, and “gain-of-function” mutations — which send the UBE3A protein into overdrive — result in enhanced degradation of its targets, including UBE3A itself. Studying the effects of these mutations could provide insight into how they affect brain development and suggest targets for therapies, says study investigator Jason Yi, assistant professor of neuroscience at Washington University in St. Louis, Missouri. Gain-of-function mutations in UBE3A can disrupt early brain development and may contribute to neurodevelopmental conditions that are distinct from Angelman syndrome, Yi and Zylka have shown in previous studies. One of the mutations they analyzed had been found in an autistic child, so the team used CRISPR to create mice with this mutation. © 2023 Simons Foundation

Keyword: Autism
Link ID: 28857 - Posted: 07.27.2023

Lilly Tozer A study that followed thousands of people over 25 years has identified proteins linked to the development of dementia if their levels are unbalanced during middle age. The findings, published in Science Translational Medicine on 19 July1, could contribute to the development of new diagnostic tests, or even treatments, for dementia-causing diseases. Most of the proteins have functions unrelated to the brain. “We’re seeing so much involvement of the peripheral biology decades before the typical onset of dementia,” says study author Keenan Walker, a neuroscientist at the US National Institute on Aging in Bethesda, Maryland. Equipped with blood samples from more than 10,000 participants, Walker and his colleagues questioned whether they could find predictors of dementia years before its onset by looking at a person’s proteome — the collection of all the proteins expressed throughout the body. They searched for any signs of dysregulation — when proteins are at levels much higher or lower than normal. The samples were collected as part of an ongoing study that began in 1987. Participants returned for examination six times over three decades, and during this time, around 1 in 5 of them developed dementia. The researchers found 32 proteins that, if dysregulated in people aged 45 to 60, were strongly associated with an elevated chance of developing dementia in later life. It is unclear how exactly these proteins might be involved in the disease, but the link is “highly unlikely to be due to just chance alone”, says Walker © 2023 Springer Nature Limited

Keyword: Alzheimers
Link ID: 28856 - Posted: 07.22.2023

Geneva Abdul The so-called “brain fog” symptom associated with long Covid is comparable to ageing 10 years, researchers have suggested. In a study by King’s College London, researchers investigated the impact of Covid-19 on memory and found cognitive impairment highest in individuals who had tested positive and had more than three months of symptoms. The study, published on Friday in a clinical journal published by The Lancet, also found the symptoms in affected individuals stretched to almost two years since initial infection. “The fact remains that two years on from their first infection, some people don’t feel fully recovered and their lives continue to be impacted by the long-term effects of the coronavirus,” said Claire Steves, a professor of ageing and health at King’s College. “We need more work to understand why this is the case and what can be done to help.” An estimated two million people living in the UK were experiencing self-reported long Covid – symptoms continuing for more than four weeks since infection – as of January 2023, according to the 2023 government census. Commonly reported symptoms included fatigue, difficulty concentrating, shortness of breath and muscle aches. The study included more than 5,100 participants from the Covid Symptom Study Biobank, recruited through a smartphone app. Through 12 cognitive tests measuring speed and accuracy, researchers examined working memory, attention, reasoning and motor controls between two periods of 2021 and 2022. © 2023 Guardian News & Media Limited or

Keyword: Learning & Memory; Attention
Link ID: 28854 - Posted: 07.22.2023

By Pam Belluck Treating Alzheimer’s patients as early as possible — when symptoms and brain pathology are mildest — provides a better chance of slowing cognitive decline, a large study of an experimental Alzheimer’s drug presented Monday suggests. The study of 1,736 patients reported that the drug, donanemab, made by Eli Lilly, can modestly slow the progression of memory and thinking problems in early stages of Alzheimer’s, and that the slowing was greatest for early-stage patients when they had less of a protein that creates tangles in the brain. For people at that earlier stage, donanemab appeared to slow decline in memory and thinking by about four and a half to seven and a half months over an 18-month period compared with those taking a placebo, according to the study, published in the journal JAMA. Among people with less of the protein, called tau, slowing was most pronounced in those younger than 75 and those who did not yet have Alzheimer’s but had a pre-Alzheimer’s condition called mild cognitive impairment, according to data presented Monday at the Alzheimer’s Association International Conference in Amsterdam. “The earlier you can get in there, the more you can impact it before they’ve already declined and they’re on this fast slope,” Dr. Daniel Skovronsky, Eli Lilly’s chief medical and scientific officer, said in an interview. “No matter how you cut the data — earlier, younger, milder, less pathology — every time, it just looks like early diagnosis and early intervention are the key to managing this disease,” he added. The findings and the recent approval of another drug that modestly slows decline in the early stages of Alzheimer’s, Leqembi, signal a potentially promising turn in the long, rocky path toward finding effective medications for Alzheimer’s, a brutal disease that plagues more than six million Americans. Donanemab is currently being considered for approval by the Food and Drug Administration. © 2023 The New York Times Company

Keyword: Alzheimers
Link ID: 28852 - Posted: 07.19.2023

Nicola Davis Science correspondent Taking part in activities such as chess, writing a journal, or educational classes in older age may help to reduce the risk of dementia, a study has suggested. According to the World Health Organization, more than 55 million people have the disease worldwide, most of them older people. However experts have long emphasised that dementia is not an inevitable part of ageing, with being active, eating well and avoiding smoking among the lifestyle choices that can reduce risk. Now researchers have revealed fresh evidence that challenging the brain could also be beneficial. Writing in the journal Jama Network Open, researchers in the US and Australia report how they used data from the Australian Aspree Longitudinal Study of Older Persons covering the period from 1 March 2010 to 30 November 2020. Participants in the study were over the age of 70, did not have a major cognitive impairment or cardiovascular disease when recruited between 2010 and 2014, and were assessed for dementia through regular study visits. In the first year, participants were asked about their social networks. They were also questioned on whether they undertook certain leisure activities or trips out to venues such as galleries or restaurants, and how frequently: never, rarely, sometimes, often or always. The team analysed data from 10,318 participants, taking into account factors such as age, sex, smoking status, education, socioeconomic status, and whether participants had other diseases such as diabetes. The results reveal that for activities such as writing letters or journals, taking educational classes or using a computer, increasing the frequency of participation by one category, for example from “sometimes” to “often”, was associated with an 11% drop in the risk of developing dementia over a 10-year period. Similarly, increased frequency of activities such as card games, chess or puzzle-solving was associated with a 9% reduction in dementia risk. © 2023 Guardian News & Media Limited

Keyword: Alzheimers; Learning & Memory
Link ID: 28851 - Posted: 07.19.2023

Lilly Tozer Injecting ageing monkeys with a ‘longevity factor’ protein can improve their cognitive function, a study reveals. The findings, published on 3 July in Nature Aging1, could lead to new treatments for neurodegenerative diseases. It is the first time that restoring levels of klotho — a naturally occurring protein that declines in our bodies with age — has been shown to improve cognition in a primate. Previous research on mice had shown that injections of klotho can extend the animals’ lives and increases synaptic plasticity2 — the capacity to control communication between neurons, at junctions called synapses. “Given the close genetic and physiological parallels between primates and humans, this could suggest potential applications for treating human cognitive disorders,” says Marc Busche, a neurologist at the UK Dementia Research Institute group at University College London. The protein is named after the Greek goddess Clotho, one of the Fates, who spins the thread of life. The study involved testing the cognitive abilities of old rhesus macaques (Macaca mulatta), aged around 22 years on average, before and after a single injection of klotho. To do this, researchers used a behavioural experiment to test for spatial memory: the monkeys had to remember the location of an edible treat, placed in one of several wells by the investigator, after it was hidden from them. Study co-author Dena Dubal, a physician-researcher at the University of California, San Francisco, compares the test to recalling where you left your car in a car park, or remembering a sequence of numbers a couple of minutes after hearing it. Such tasks become harder with age. The monkeys performed significantly better in these tests after receiving klotho — before the injections they identified the correct wells around 45% of the time, compared with around 60% of the time after injection. The improvement was sustained for at least two weeks. Unlike in previous studies involving mice, relatively low doses of klotho were effective. This adds an element of complexity to the findings, which suggests a more nuanced mode of actions than was previously thought, Busche says. © 2023 Springer Nature Limited

Keyword: Learning & Memory; Development of the Brain
Link ID: 28847 - Posted: 07.06.2023

By Tammy Worth In two decades as a pediatrician, Jason Reynolds has had no success treating patients with opioid use disorder by sending them to rehab. But five years ago, when his Massachusetts practice, Wareham Pediatric Associates PC, became the first in the state to offer medication therapy to adolescent patients, he saw dramatic results. The first patient he treated with medication, a young man named Nate, had overdosed on opioids twice in the 24-hour period before seeing Reynolds. But that patient has had no opioid relapses since starting drug therapy. Reynolds’ success received a lot of media attention, and one interviewer, he recalls, asked Nate if any of his friends would also consider starting the treatment. Reynolds is among a small minority of pediatricians using medication to treat opioid use disorder in adolescents. Fewer than 2 percent of all physicians prescribing the medications are pediatricians, and many youth rehabilitation facilities don’t offer them at all. Medication for opioid use disorder (MOUD) uses buprenorphine or methadone to reduce cravings and withdrawal symptoms, or naltrexone to block the high that users would otherwise get if they decided to use opioids. Though MOUD is often used to treat adults, several barriers have prevented it from being adopted more widely for youth. Reynolds and a handful of other practitioners across the country are now working to provide education and training to other health care providers, hoping to increase use of this life-saving treatment. Opioid use among US youth is on the rise nationally, with diagnoses increasing from 0.26 per 100,000 person-years in 2001 to 1.51 in 2014. Overdose deaths have also spiked, more than doubling among youth ages 14 to 18, from 492 in 2019 to 1,146 in 2021. © 2023 Annual Reviews

Keyword: Drug Abuse; Development of the Brain
Link ID: 28844 - Posted: 07.06.2023

By Claudia Lopez Lloreda There are plenty of reasons to get off your duff and exercise—but is improving your brain one of them? The U.S. Centers for Disease Control and Prevention touts exercise as a way to “boost brain health,” while the World Health Organization suggests that about 2 hours of moderate activity or 75 minutes of vigorous activity per week can help improve thinking and memory skills. But new research reveals a more complex picture. One recent review of the literature suggests the studies tying exercise to brain health may have important limitations, including small sample sizes. Other studies suggest there is no one-size-fits-all approach to exercising as a way to boost cognition or prevent age-related cognitive decline. Still others indicate exercise may actually be harmful in people with certain medical conditions. Here’s the latest on what we know. What is the science linking exercise and improved brain function? Many studies correlate participants’ self-reported exercise with scores on cognitive tests, or track the effects of randomizing participants into groups that either exercise or remain sedentary. They typically find that the more physical activity a person does, the better their cognition. This result holds for healthy people, stroke survivors, and those with other neurological conditions such as Alzheimer’s disease. A study published earlier this year relied on genetic data to explore the effects of exercise. A team led by sports scientist Boris Cheval at the University of Geneva grouped about 350,000 people in the United Kingdom according to genetic variants associated with more or less physical activity. Those with an apparent genetic predisposition to be more active also tended to perform better on a set of cognitive tests, the researchers concluded in Scientific Reports. Other studies have focused on age-related cognitive decline. Research published in February in the Journal of Neurology, Neurosurgery & Psychiatry tracked more than 1400 people for 30 years, showing that more physical activity was associated with better cognitive performance at age 69.

Keyword: Development of the Brain; Alzheimers
Link ID: 28838 - Posted: 07.01.2023

Nicola Davis Taking a short nap during the day may help to protect the brain’s health as it ages, researchers have suggested after finding that the practice appears to be associated with larger brain volume. While previous research has suggested long naps could be an early symptom of Alzheimer’s disease, other work has revealed that a brief doze can improve people’s ability to learn. Now researchers say they have found evidence to suggest napping may help to protect against brain shrinkage. That is of interest, the team say, as brain shrinkage, a process that occurs with age, is accelerated in people with cognitive problems and neurodegenerative diseases, with some research suggesting this may be related to sleep problems. “In line with these studies, we found an association between habitual daytime napping and larger total brain volume, which could suggest that napping regularly provides some protection against neurodegeneration through compensating for poor sleep,” the researchers note. Writing in the journal Sleep Health, researchers at UCL and the University of the Republic in Uruguay report how they drew on data from the UK Biobank study that has collated genetic, lifestyle and health information from 500,000 people aged 40 to 69 at recruitment. The team used data from 35,080 Biobank participants to look at whether a combination of genetic variants that have previously been associated with self-reported habitual daytime napping are also linked to brain volume, cognition and other aspects of brain health. © 2023 Guardian News & Media Limited

Keyword: Sleep; Development of the Brain
Link ID: 28829 - Posted: 06.21.2023

By Harrison Smith As a young boy in small-town Mississippi, Donald Triplett was oddly distant, with no apparent interest in his parents or anyone else who tried to make conversation. He was obsessed with spinning round objects and had an unusual way of speaking, substituting “you” for “I” and repeating words like “business” and “chrysanthemum.” He also showed a savant-like brilliance, naming notes as they were played on the piano and performing mental calculations with ease. When a visitor asked “87 times 23,” he didn’t hesitate before answering — correctly — “2,001.” Mr. Triplett would make medical history as “Case 1,” the first person formally diagnosed with autism. His upbringing and behavior were described at length in a 1943 scientific article by Austrian American psychiatrist Leo Kanner, “Autistic Disturbances of Affective Contact,” which outlined the developmental disability now known as autism spectrum disorder, or ASD. The article went on to describe 10 other autistic children, most of whom were locked away in state schools and hospitals while experiencing communication and behavior challenges. Checking in with his former subjects almost 30 years later, Kanner would write that institutionalization was “tantamount to a life sentence … a total retreat to near-nothingness.” Mr. Triplett, by contrast, gained acceptance and admiration while remaining a part of his community. With support from his family, which could afford to send him to Kanner and which later set up a trust fund to look after him, he graduated from college, got a job as a bank teller and found companionship in a morning coffee club at City Hall. He played golf, sang in a choir and traveled the world, visiting at least three-dozen countries and making it to Hawaii 17 times. By choice, he traveled alone, surprising relatives when he would announce at Sunday dinner that he had recently returned from seeing a golf tournament in California or, in search of an oyster dinner, driven his Cadillac to New Orleans.

Keyword: Autism
Link ID: 28826 - Posted: 06.21.2023

By Claudia Lopez Lloreda A baby born through the vaginal canal picks up critical microbes along the way that help it stay healthy later in life. But babies delivered via cesarean section miss out on those useful, gut-colonizing bacteria, which may put them at greater risk of developing certain health conditions and developmental disorders. Now, researchers at Southern Medical University say that by exposing C-section babies to the microbes they’ve missed—an intervention called vaginal seeding—doctors can partially restore these missing gut bacteria. The procedure may even aid in their early development. Newborns delivered via C-section who received their mother’s vaginal microbes had more advanced motor and communication skills than other C-section babies months later, the team reports today in Cell Host & Microbe. But some clinicians argue these benefits for infants have not yet been proved, nor has the procedure’s safety. “This study establishes a link showing that there is a possible benefit in a select group of infants and mothers,” says Mehreen Zaigham, an obstetrician at Lund University who was not involved in the study. “But it has to be proven with larger longitudinal studies.” The microbiomes of C-section babies look a lot different from those of babies born vaginally. In particular, they have lower numbers of Lactobacillus, Escherichia, and Bacteroides bacteria in their guts. These microbes are believed to be critical for growth and are thought to help protect against asthma, allergies, obesity, and autoimmune disorders—all conditions that are more common among C-section babies. A few highly controversial studies have suggested some babies delivered by C-section may be at a greater risk of developing neurodevelopmental conditions such as autism spectrum disorder, which some researchers attribute to their disrupted microbiome. Other researchers have roundly criticized that suggestion, however. To restore the microbiomes of infants delivered by C-section, researchers have come up with a simple solution: Swab them with bacteria from their mother’s vagina shortly after they are born. This method, called vaginal seeding, was first clinically tested 7 years ago by Jose Clemente, a geneticist at the Icahn School of Medicine at Mount Sinai, and Maria Gloria Dominguez Bello, a microbial ecologist at Rutgers University, who found the procedure indeed restored microbes that C-section babies lacked. However, these results were based on a small group of just 11 babies.

Keyword: Development of the Brain; Neuroimmunology
Link ID: 28824 - Posted: 06.17.2023

Kerri Smith In a dimly lit laboratory in London, a brown mouse explores a circular tabletop, sniffing as it ambles about. Suddenly, silently, a shadow appears. In a split second, the mouse’s brain whirs with activity. Neurons in its midbrain start to fire, sensing the threat of a potential predator, and a cascade of activity in an adjacent region orders its body to choose a response — freeze to the spot in the hope of going undetected, or run for shelter, in this case a red acetate box stationed nearby. From the mouse’s perspective, this is life or death. But the shadow wasn’t cast by a predator. Instead, it is the work of neuroscientists in Tiago Branco’s lab, who have rigged up a plastic disc on a lever to provoke, and thereby study, the mouse’s escape behaviour. This is a rapid decision-making process that draws on sensory information, previous experience and instinct. Branco, a neuroscientist at the Sainsbury Wellcome Centre at University College London, has wondered about installing a taxidermied owl on a zip wire to create a more realistic experience. And his colleagues have more ideas — cutting the disc into a wingspan shape, for instance. “Having drones — that would also be very nice,” says Dario Campagner, a researcher in Branco’s lab. A mouse detects a looming threat and runs for cover. The shadow has been darkened. The set-up is part of a growing movement to step away from some of the lab experiments that neuroscientists have used for decades to understand the brain and behaviour. Such exercises — training an animal to use a lever or joystick to get a reward, for example, or watching it swim through a water maze — have established important principles of brain activity and organization. But they take days to months of training an animal to complete specific, idiosyncratic tasks. The end result, Branco says, is like studying a “professional athlete”; the brain might work differently in the messy, unpredictable real world. Mice didn’t evolve to operate a joystick. Meanwhile, many behaviours that come naturally — such as escaping a predator, or finding scarce food or a receptive mate — are extremely important for the animal, says Ann Kennedy, a theoretical neuroscientist at Northwestern University in Chicago, Illinois. They are “critical to survival, and under selective pressure”, she says. By studying these natural actions, scientists are hoping to glean lessons about the brain and behaviour that are more holistic and more relevant to everyday activity than ever before.

Keyword: Learning & Memory; Evolution
Link ID: 28822 - Posted: 06.14.2023

By Jordan Kinard Long the fixation of religions, philosophy and literature the world over, the conscious experience of dying has recently received increasingly significant attention from science. This comes as medical advances extend the ability to keep the body alive, steadily prying open a window into the ultimate locked room: the last living moments of a human mind. “Around 1959 humans discovered a method to restart the heart in people who would have died, and we called this CPR,” says Sam Parnia, a critical care physician at NYU Langone Health. Parnia has studied people’s recollections after being revived from cardiac arrest—phenomena that he refers to as “recalled experiences surrounding death.” Before CPR techniques were developed, cardiac arrest was basically synonymous with death. But now doctors can revive some people up to 20 minutes or more after their heart has stopped beating. Furthermore, Parnia says, many brain cells remain somewhat intact for hours to days postmortem—challenging our notions of a rigid boundary between life and death. Advancements in medical technology and neuroscience, as well as shifts in researchers’ perspectives, are revolutionizing our understanding of the dying process. Research over the past decade has demonstrated a surge in brain activity in human and animal subjects undergoing cardiac arrest. Meanwhile large surveys are documenting the seemingly inexplicable periods of lucidity that hospice workers and grieving families often report witnessing in people with dementia who are dying. Poet Dylan Thomas famously admonished his readers, “Do not go gentle into that good night. Rage, rage against the dying of the light.” But as more resources are devoted to the study of death, it is becoming increasingly clear that dying is not the simple dimming of one’s internal light of awareness but rather an incredibly active process in the brain. © 2023 Scientific American,

Keyword: Attention; Development of the Brain
Link ID: 28820 - Posted: 06.14.2023

Kari Paul and Maanvi Singh Elon Musk’s brain-implant company Neuralink last week received regulatory approval to conduct the first clinical trial of its experimental device in humans. But the billionaire executive’s bombastic promotion of the technology, his leadership record at other companies and animal welfare concerns relating to Neuralink experiments have raised alarm. “I was surprised,” said Laura Cabrera, a neuroethicist at Penn State’s Rock Ethics Institute about the decision by the US Food and Drug Administration to let the company go ahead with clinical trials. Musk’s erratic leadership at Twitter and his “move fast” techie ethos raise questions about Neuralink’s ability to responsibly oversee the development of an invasive medical device capable of reading brain signals, Cabrera argued. “Is he going to see a brain implant device as something that requires not just extra regulation, but also ethical consideration?” she said. “Or will he just treat this like another gadget?” Neuralink is far from the first or only company working on brain interface devices. For decades, research teams around the world have been exploring the use of implants and devices to treat conditions such as paralysis and depression. Already, thousands use neuroprosthetics like cochlear implants for hearing. But the broad scope of capabilities Musk is promising from the Neuralink device have garnered skepticism from experts. Neuralink entered the industry in 2016 and has designed a brain-computer interface (BCI) called the Link – an electrode-laden computer chip that can be sewn into the surface of the brain and connects it to external electronics – as well as a robotic device that implants the chip. © 2023 Guardian News & Media Limited

Keyword: Robotics; Learning & Memory
Link ID: 28816 - Posted: 06.07.2023